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The Journal of Immunology, 1979, 123: 1097-1105.
Copyright © 1979 by The American Association of Immunologists, Inc.

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Cellular and Humoral Immune Reactivity to Tumor-Associated Antigens in Chickens Infected with Rous Sarcoma Virus1

Michael R. Hall, Louis F. Qualtiere and Paul Meyers2

Department of Microbiology, Mayo Clinic and Mayo Medical School, Rochester, Minnesota 55901

Abstract

With a leukocyte blastogenesis assay and 3 M KCl extracts of chicken cells infected or infected and transformed by various avian tumor viruses (ATV), the time course of development of cellular reactivity in RSV tumor-bearing chickens to antigens expressed on these cell types was examined. Leukocyte reactivity to mitogens in RSV-injected birds was also investigated. Similarly, humoral responses to ATV-antigens and virus-induced antigens were assessed over time, by measuring the development of antiviral neutralizing antibody, as well as antibody to cell surface antigens on various cell types, by means of an isotopic antiglobulin test (IAT). There were no differences in phytohemmaglutinin responsiveness between the leukocytes of RSV-injected birds and control birds, but responses to pokeweed mitogen were sometimes elevated in RSV-injected animals. Cellular immunity to 3 M KCl extracts, principally to those extracts containing structural components of the virus envelope, developed between 3 and 5 weeks post-injection, during tumor growth and regression, and then declined, although the immune response could be restimulated by virus rechallenge. For the most part, responses to nonvirion tumor-specific surface antigen (TSSA) was weak except after RSV rechallenge. Humoral reactivity as measured by IAT also seemed to correlate well with the presence of virus envelope antigens (VEA) on infected indicator cells and appeared before antiviral neutralizing antibody. The data indicated that, at least during the primary response, major immune reactivity in RSV-injected birds appeared to be directed against VEA and that TSSA appeared to be most immunogenic when VEA was also present.

Footnotes

1 This work was supported by Public Health Service Grant CA15494 from the National Cancer Institute and by Mayo Foundation.

2 Address requests for reprints to Dr. Meyers.







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